New research shows that when mitochondria are transplanted from astrocytes to damaged neurons after a brain hemorrhage, they promote healing. The healthy mitochondria from the astrocytes stimulate the production of a free-radical-fighting enzyme, manganese superoxide dismutase (Mn-SOD), in the neurons, which reduces oxidative stress and neuronal death.

The work, which was led by Joo Eun Jung, PhD, an assistant professor in the department of neurology at the University of Texas Health Science Center at Houston, McGovern Medical School, was published in The Journal of Neuroscience (“Transplantation of astrocytic mitochondria modulates neuronal antioxidant defense and neuroplasticity and promotes functional recovery after intracerebral hemorrhage”).

During intracerebral hemorrhage (ICH), an artery in the brain bursts, damaging mitochondria and releasing free radicals that cause even more damage.

Astrocytes are known to promote recovery after ICH by releasing functional mitochondria into adjacent microglia. But, until this study, the role of mitochondrial transfer from astrocytes to neurons was unclear.

“[We] show that systemic transplantation of astrocytic [mitochondria] restores ICH-impaired neuronal anti-oxidative defense, enhances neurite outgrowth, and improves stroke recovery after ICH,” wrote the researchers in their paper.

The research team induced a brain hemorrhage in mice. The hemorrhage reduced levels of Mn-SOD in the brain and increased the number of free radicals. “[We] found that ICH causes a robust increase in superoxide generation and elevated oxidative damage that coincides with loss of the mitochondrial enzyme [Mn-SOD],” the researchers wrote.

The team then injected the mice with healthy mitochondria. Using molecular tags, the researchers found that the rodents’ neurons took up the mitochondria from the bloodstream.

The mice who received the healthy mitochondria showed improved neurological recovery. “The damaging effect of ICH was reversed by intravenous transplantation of astrocytic [mitochondria] that upon entering the brain (and neurons), restored Mn-SOD levels and reduced neurological deficits in male mice subjected to ICH,” they wrote. Furthermore, the benefits decreased if the mice received mitochondria without the Mn-SOD enzyme.

“Using an in vitro ICH-like injury model in cultured neurons, we established that astrocytic [mitochondria] upon entering neurons prevented reactive oxygen species-induced oxidative stress and neuronal death by restoring neuronal Mn-SOD levels, while at the same time promoted neurite extension and upregulation of synaptogenesis-related gene expression,” they continued. “Furthermore, we found that [mitochondria] genome-encoded small peptide humanin (HN) that is normally abundant in [mitochondria], could simulate [mitochondria]-transfer effect on neuronal Mn-SOD expression, oxidative stress, and neuroplasticity under ICH-like injury.”

These results reveal that healthy mitochondria may improve health and aid recovery of damaged neurons in the brain. “Our study suggests that systemic transplantation of astrocytic [mitochondria] could be considered as a novel and potentially promising strategy for ICH treatment,” they concluded.

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